Furthermore, mice with cardiac-specific overexpression of mutated human αB-crystallin (hR120GCryAB) displayed increases in GSH levels and in activities of GR, glucose-6-phosphate dehydrogenase (G6PD), catalase, and GPx (indicative of reductive stress), which led to the development of cardiac hypertrophy and heart failure in these mice (77, 78). The gene discussed is G6PD; the disease is heart failure.